Front. Bioeng. Biotechnol. Frontiers in Bioengineering and Biotechnology Front. Bioeng. Biotechnol. 2296-4185 Frontiers Media S.A. 10.3389/fbioe.2020.598323 Bioengineering and Biotechnology Correction Corrigendum: Molecular Insights Into Lysyl Oxidases in Cartilage Regeneration and Rejuvenation Lin Weiping 1 * † Xu Liangliang 2 † Li Gang 1 3 * 1Department of Orthopaedics and Traumatology, Stem Cells and Regenerative Medicine Laboratory, Li Ka Shing Institute of Health Sciences, The Chinese University of Hong Kong, Prince of Wales Hospital, Hong Kong, China 2The First Affiliated Hospital of Guangzhou University of Chinese Medicine, Lingnan Medical Research Center, Guangzhou University of Chinese Medicine, Guangzhou, China 3MOE Key Laboratory for Regenerative Medicine, School of Biomedical Sciences, The Chinese University of Hong Kong, Hong Kong, China *Correspondence: Gang Li gangli@cuhk.edu.hk Weiping Lin weipinglin@link.cuhk.edu.hk

Approved by: Frontiers Editorial Office, Frontiers Media SA, Switzerland

This article was submitted to Preclinical Cell and Gene Therapy, a section of the journal Frontiers in Bioengineering and Biotechnology

†These authors have contributed equally to this work

 26 10 2020 2020 8 598323 24 08 2020 25 08 2020 Copyright © 2020 Lin, Xu and Li. 2020 Lin, Xu and Li

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 A Corrigendum on Molecular Insights Into Lysyl Oxidases in Cartilage Regeneration and Rejuvenation by Lin, W., Xu, L., and Li, G. (2020). Front. Bioeng. Biotechnol. 8:359. doi: 10.3389/fbioe.2020.00359 lysyl oxidase cartilage hypoxia-inducible factor copper transcription activity regeneration rejuvenation

In the original article, there was a mistake in Figure 4 as published. The corrected Figure 4 and figure legend appear below.

Schematic illustration of copper-mediated hypoxia-response element (HRE)-directed transcriptional fine-tuning of cartilage homeostasis-associated genes in chondrocytes. Under normoxia, HIF-1α undergoes PHDs-mediated prolyl hydroxylation, and prolyl OH HIF-1α is ligated by pVHL, an E3 ubiquitin ligase, and degraded by the proteasome finally. Copper stabilizes HIF-1α protein by inhibiting PHDs activity in an iron-independent manner. Under hypoxia or through interaction with HSP90, HIF-1α stabilizes and accumulates in the cell nucleus, where it forms a dimer with the HIF-1β subunit and a putative unidentified copper-chaperone. The dimer then forms a transcriptional complex with coactivator CBP/p300 through binding with HRE, regulating the expression of various downstream target genes, such as LOXL2, SOX9, and VEGF. Simultaneously, SOX9 is a negative regulator of VEGF, whilst the expression of SOX9 target genes (i.e., Type II collagen, and Aggrecan) is initiated, which is essential for cartilage synthesis and survival during both embryonic joint development and cartilage homeostasis. HIF-1α, hypoxia-inducible factor-1α; PHDs, prolyl hydroxylases; OH: enzymatic hydroxylation; pVHL, von Hippel-Lindau tumor suppressor protein; HRE, hypoxia-response element; Ub, ubiquitinated; SOX9, SRY (sex determining region Y)-box 9; HSP90, heat shock protein 90; LOXL2, lysyl oxidase-like 2; VEGF, vascular endothelial growth factor; Cu, copper.

The authors apologize for this error and state that they do not change the scientific conclusions of the article in any way. The original article has been updated.